Nature Reviews Nephrology最新文献

Closing the gap: disparities in access to and implementation of guideline-directed medical therapy for CKM syndrome. 缩小差距：CKM综合征指导医学治疗的可及性和实施方面的差异

IF 46.7 1区医学

Nature Reviews Nephrology Pub Date : 2026-10-16 DOI: 10.1038/s41581-026-01136-3

Magdalena Madero

引用次数: 0

Infection-associated acute kidney injury in resource-limited settings. 资源有限环境中感染相关的急性肾损伤

IF 46.7 1区医学

Nature Reviews Nephrology Pub Date : 2026-10-15 DOI: 10.1038/s41581-026-01138-1

Michael T Hawkes, Anthony Batte, Lakhmir S Chawla, Andrea L Conroy

{"title":"Infection-associated acute kidney injury in resource-limited settings.","authors":"Michael T Hawkes, Anthony Batte, Lakhmir S Chawla, Andrea L Conroy","doi":"10.1038/s41581-026-01138-1","DOIUrl":"https://doi.org/10.1038/s41581-026-01138-1","url":null,"abstract":"Acute kidney injury (AKI) is a frequent and life-threatening complication of infection, and a major contributor to preventable morbidity and mortality in resource-limited settings. In these contexts, AKI is commonly driven by a broad range of infections, including enteric, zoonotic and vector-borne diseases, that occur outside the hospital and in populations with limited access to diagnostics and supportive care. Infection-associated AKI results from diverse and overlapping mechanisms, including hypovolaemia, inflammation, endothelial and microcirculatory dysfunction, haemolysis and direct kidney involvement, and is increasingly shaped by environmental stressors such as heat exposure and climate-related disruptions that amplify dehydration, infection risk and kidney injury. Susceptibility to AKI is further influenced by reduced kidney reserve, which reflects nephron endowment and prior kidney injury, and can be silently depleted by severe or recurrent insults. Repeated infectious exposures and incomplete recovery from AKI might affect long-term kidney health and survival, but these trajectories remain poorly characterized. Challenges in timely recognition of both AKI and infections contribute to delayed treatment and worse outcomes, particularly among vulnerable populations. Strengthening infection prevention, improving context-appropriate diagnostics for AKI and infection, minimizing iatrogenic kidney injury, addressing environmental drivers and developing affordable scalable kidney replacement therapies are essential to reducing inequities and improving long-term kidney health globally.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":" ","pages":""},"PeriodicalIF":46.7,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149195695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cardiovascular-kidney-metabolic syndrome and cancer. 心血管肾代谢综合征和癌症。

IF 46.7 1区医学

Nature Reviews Nephrology Pub Date : 2026-10-13 DOI: 10.1038/s41581-026-01142-5

Parta Hatamizadeh, Kenar D Jhaveri

引用次数: 0

The case for cardiovascular-kidney-liver-metabolic syndrome. 心血管-肾-肝-代谢综合征的病例。

IF 46.7 1区医学

Nature Reviews Nephrology Pub Date : 2026-10-08 DOI: 10.1038/s41581-026-01137-2

John Cijiang He, Kyung Lee

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Sex and gender in cardiovascular–kidney–metabolic health: strengthening the evidence 性与性别在心血管-肾脏-代谢健康中的关系：强化证据

IF 41.5 1区医学

Nature Reviews Nephrology Pub Date : 2026-10-06 DOI: 10.1038/s41581-026-01141-6

Sofia B. Ahmed

引用次数: 0

Preventative nephrology in the cardiovascular–kidney–metabolic era 心血管-肾脏代谢时代的预防性肾脏病学

IF 41.5 1区医学

Nature Reviews Nephrology Pub Date : 2026-10-05 DOI: 10.1038/s41581-026-01140-7

Hellena Hailu Habte-Asres,David C. Wheeler

引用次数: 0

Metabolic control by liver–kidney crosstalk and glucagon in health and disease 健康和疾病中由肝肾串扰和胰高血糖素控制的代谢。

IF 46.7 1区医学

Nature Reviews Nephrology Pub Date : 2026-09-29 DOI: 10.1038/s41581-026-01111-y

Volker Vallon, Nicolai J. Wewer Albrechtsen

{"title":"Metabolic control by liver–kidney crosstalk and glucagon in health and disease","authors":"Volker Vallon, Nicolai J. Wewer Albrechtsen","doi":"10.1038/s41581-026-01111-y","DOIUrl":"10.1038/s41581-026-01111-y","url":null,"abstract":"Gluconeogenesis, nitrogen metabolism and acid–base regulation are fundamental for the maintenance of metabolic homeostasis. These three processes form an interconnected triangle, with liver–kidney crosstalk and the hormone glucagon at its core. Both kidney and liver perform gluconeogenesis, and they function in co-ordination to regulate the formation and excretion of the organic osmolyte urea and the acid equivalent ammonium, and to determine the usage and de novo generation of bicarbonate. Within the liver, glucagon promotes fasting-induced gluconeogenesis and the bicarbonate-consuming formation of urea from amino acid-derived ammonia in response to protein intake and catabolic states. Within the kidney, glucagon facilitates the excretion of urea. In metabolic acidosis, the liver shifts nitrogen metabolism from ureagenesis to glutamine formation for kidney ammoniagenesis. Liver and kidney disease interfere with whole-body homeostasis of glucose, nitrogen and acid–base by promoting hypo- or hyperglycaemia, ammonia and urea toxicity, and metabolic alkalosis or acidosis. Inhibitors of the sodium glucose cotransporter SGLT2 not only cause glucosuria and compensatory hepatic gluconeogenesis but also interfere with kidney bicarbonate reabsorption, leading to compensatory kidney ammoniagenesis, bicarbonate formation and gluconeogenesis, which mitigates lactate accumulation and is associated with improved kidney health. Glucagon receptor agonists, in combination with GLP1 receptor agonists, also hold therapeutic promise in obesity and fatty liver and potentially kidney disease, but a better understanding of their effects is needed in the pathophysiological setting. Gluconeogenesis, nitrogen metabolism and acid–base regulation are fundamental for the maintenance of metabolic homeostasis. This Review describes how these processes form an interconnected triangle, with liver–kidney crosstalk and the hormone glucagon at its core, and discusses how changes in these processes contribute to kidney, liver and metabolic disease.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"22 11","pages":"765-783"},"PeriodicalIF":46.7,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Targeting the aldosterone-mineralocorticoid receptor pathway in cardiovascular-kidney-metabolic syndrome. 心血管-肾-代谢综合征中醛固酮-矿皮质激素受体通路的研究。

IF 46.7 1区医学

Nature Reviews Nephrology Pub Date : 2026-09-28 DOI: 10.1038/s41581-026-01125-6

Tania Sánchez-Bayuela, Jonatan Barrera-Chimal, Frederic Jaisser

{"title":"Targeting the aldosterone-mineralocorticoid receptor pathway in cardiovascular-kidney-metabolic syndrome.","authors":"Tania Sánchez-Bayuela, Jonatan Barrera-Chimal, Frederic Jaisser","doi":"10.1038/s41581-026-01125-6","DOIUrl":"https://doi.org/10.1038/s41581-026-01125-6","url":null,"abstract":"The concept of cardiovascular-kidney-metabolic (CKM) syndrome integrates cardiovascular, kidney and metabolic disorders into a single pathophysiological continuum characterized by chronic inflammation, oxidative stress, fibrosis and progressive organ dysfunction. A central driver of CKM syndrome progression is inappropriate activation of the aldosterone-mineralocorticoid receptor (MR) pathway, which promotes adverse remodelling of the heart, kidney, vasculature, adipose tissue, liver and pancreas. Steroidal MR antagonists (MRAs) and non-steroidal MRAs mitigate maladaptive MR signalling and improve cardiorenal outcomes. Compared with steroidal MRAs, non-steroidal MRAs such as finerenone provide enhanced tissue selectivity and favourable safety profiles. Finerenone has been shown to reduce cardiovascular and renal events in patients with chronic kidney disease (CKD) and in patients with heart failure. Aldosterone synthase inhibitors represent a complementary approach that suppresses aldosterone production upstream of MR activation and has shown promising results in resistant hypertension and CKD. Preclinical and clinical data indicate that combined strategies targeting the aldosterone-MR axis can attenuate cardiorenal remodelling, insulin resistance and organ injury, offering a comprehensive therapeutic approach. Ongoing trials will clarify the efficacy of these combined therapies in non-diabetic CKD, resistant hypertension and broader CKM syndrome populations. Overall, targeting the aldosterone-MR pathway represents a central strategy to reduce organ dysfunction, improve metabolic homeostasis and limit progression of CKM syndrome.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":" ","pages":""},"PeriodicalIF":46.7,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149075269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Recommendations for the management of frailty in chronic kidney disease: a consensus report 慢性肾脏疾病虚弱管理建议：一份共识报告

IF 41.5 1区医学

Nature Reviews Nephrology Pub Date : 2026-09-25 DOI: 10.1038/s41581-026-01128-3

Philip Kam-Tao Li,Gordon Chun-Kau Chan,Mara McAdams-DeMarco,Stephanie Thompson,Marjolijn van Buren,Andrew C. Nixon,Jack Kit-Chung Ng,Ruth E. Hubbard,Sarbjit Vanita Jassal,Chia-Ter Chao,Kai-Ming Chow,Melanie Dani,Jessica Dawson,Barnaby Hole,Yoshitaka Isaka,Vivekanand Jha,Ann M. O’Hare,Na Tian,Marcello Tonelli,Bill Wang,Nicola Wearne,Jean Woo,Guang-Yan Cai,Brett Cullis,Rasheeda K. Hall,Alice L. Kennard,Edwina A. Brown,Sara N. Davison,David W. Johnson

引用次数: 0

An integrated single-cell atlas of hypertension 高血压的综合单细胞图谱。

IF 46.7 1区医学

Nature Reviews Nephrology Pub Date : 2026-09-24 DOI: 10.1038/s41581-026-01135-4

Susan J. Allison

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